Medullary sympathoexcitatory neurons are inhibited by activation of the medial prefrontal cortex in the rat

1996 ◽  
Vol 270 (4) ◽  
pp. R713-R719 ◽  
Author(s):  
A. J. Verberne
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Prefrontal Cortex ◽  
Arterial Blood Pressure ◽  
Medial Prefrontal Cortex ◽  
Sympathetic Nerve ◽  
Ventrolateral Medulla ◽  
Arterial Blood ◽  
Stimulation Of ◽  
Nerve Discharge

Electrical stimulation of the medial prefrontal cortex (MPFC) reduces arterial blood pressure. To investigate the mechanism of this response, the effects of electrical and chemical stimulation of the MPFC on splanchnic and lumbar sympathetic nerve discharge and on the discharges of barosensitive neurons of the rostral ventrolateral medulla (RVLM) were studied in halothane-anesthetized rats. Electrical stimulation (20 Hz, 1 ms, 100 and sympathoinhibitory responses (reduced discharge of the splanchnic sympathetic nerve). Microinjection of glutamate (10 nmol/100 nl) into the MPFC also reduced arterial blood pressure and sympathetic discharge. Electrical stimulation (0.5 Hz, 1-ms pulse pairs, 3-ms interval, 150-300 microA) produced distinct patterns of splanchnic and lumbar sympathetic nerve discharge. A clear sympathoinhibitory phase with an onset latency of 146 +/- 14 ms was observed only in the case of the splanchnic sympathetic nerve activity. Electrical stimulation at depressor sites within the MPFC also inhibited the discharge of 10 of 21 RVLM barosensitive neurons tested. RVLM neurons were never excited by MPFC stimulation. These results indicate that the MPFC contains neurons that form part of a central sympathoinhibitory pathway.

Cuneiform nucleus stimulation produces activation of medullary sympathoexcitatory neurons in rats

1995 ◽  
Vol 268 (3) ◽  
pp. R752-R758 ◽  
Author(s):  
A. J. Verberne
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Arterial Blood Pressure ◽  
Ventrolateral Medulla ◽  
Onset Latency ◽  
Thoracic Spinal Cord ◽  
Arterial Blood ◽  
Thoracic Spinal ◽  
Cuneiform Nucleus ◽  
Stimulation Of

Activation of the cuneiform nucleus (CNF) of the midbrain produces elevation of arterial blood pressure. This study examined the influence of the CNF on arterial blood pressure, sympathetic vasomotor outflow, and the discharges of barosensitive sympathoexcitatory neurons of the rostral ventrolateral medulla (RVLM) in halothane-anesthetized, paralyzed rats. Electrical stimulation (50 Hz, 25-75 microA, 10 s) of the CNF elicited intensity-dependent elevations in arterial blood pressure associated with excitation of the sympathetic vasomotor discharge (elevated discharge of the lumbar sympathetic nerve). Intermittent paired-pulse electrical stimulation of the CNF elicited an excitatory response in the discharge of the lumbar sympathetic outflow that consisted of an early peak (onset latency 84 +/- 4 ms) and a smaller late peak (onset latency 217 +/- 6 ms). Seventeen of 22 RVLM sympathoexcitatory neurons tested were excited by stimulation of the CNF. Twelve of 14 units tested projected to the thoracic spinal cord, and of these, 10 units were excited by CNF stimulation with an onset latency of 16 +/- 1 ms. These findings support the hypothesis that the sympathoexcitatory and pressor responses elicited by activation of the CNF are mediated by RVLM sympathoexcitatory neurons.

PREFERENTIAL RELEASE OF OXYTOCIN FROM THE NEUROHYPOPHYSIS AFTER ELECTRICAL STIMULATION OF THE AFFERENT PATH OF THE MILK-EJECTION REFLEX IN THE BRAIN OF THE GUINEA-PIG

1968 ◽  
Vol 40 (2) ◽  
pp. 205-214 ◽  
Author(s):  
J. S. TINDAL ◽  
G. S. KNAGGS ◽  
A. TURVEY
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Guinea Pig ◽  
Arterial Blood Pressure ◽  
Pituitary Stalk ◽  
Milk Ejection ◽  
Arterial Blood ◽  
Milk Ejection Reflex ◽  
The Brain ◽  
Stimulation Of

SUMMARY Discrete portions of the afferent path of the milk-ejection reflex have been explored in the brain of the lactating guinea-pig. Both intramammary pressure and arterial blood pressure were recorded to detect release of oxytocin and vasopressin. It was found that the milk-ejection responses which occurred after electrical stimulation of the pathway in the midbrain and hypothalamus were caused by the release of oxytocin without detectable release of vasopressin. A mixture of oxytocin and vasopressin, in the ratio of approximately 3:1, was released only after electrical stimulation of the rostral tuberal region of the hypothalamus adjacent to the pituitary stalk. It is concluded that the afferent path in the brain of the guinea-pig studied is concerned with the preferential release of oxytocin from the neurohypophysis and that it is the pathway of the milk-ejection reflex.

Tonic influences from the rostral medulla affect sympathetic nerves differentially

1989 ◽  
Vol 256 (2) ◽  
pp. R323-R331 ◽  
Author(s):  
C. P. Yardley ◽  
R. D. Stein ◽  
L. C. Weaver
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Sympathetic Nerves ◽  
Ventrolateral Medulla ◽  
Renal Nerves ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Tonically Active Neurons ◽  
Nerve Discharge

Tonically active neurons in the rostral ventrolateral medulla (RVLM) that project to the autonomic regions of the spinal cord are essential for maintenance of arterial blood pressure at normal levels. Microinjection of glycine into the RVLM in anesthetized cats to inhibit the tonic discharge of these neurons caused variable initial responses in renal and mesenteric nerve discharge and arterial blood pressure. These initial responses were consistently followed by more prolonged decreases in renal and mesenteric nerve discharge and decreases in arterial blood pressure. The tonic influences of neurons in the RVLM were found to be distributed unequally to sympathetic nerves because activity of renal nerves was decreased significantly more than that of mesenteric nerves. The variable nerve and cardiovascular responses during the first 1-3 min after glycine injection were not solely due to loading or unloading of baroreceptors because similar initial responses were seen in vagotomized and sinoaortic denervated cats. Additionally, when muscimol was microinjected into the same sites, only consistent and prolonged decreases in nerve discharge and blood pressure occurred. The inhibitory actions of muscimol on RVLM neurons caused significantly greater decreases in renal than mesenteric nerve activity. Together, these findings demonstrate that the tonic discharge of neurons in the RVLM has unequal influences on renal and mesenteric nerves.

Lack of involvement of GABA in baroreceptor-mediated sympathoinhibition

1986 ◽  
Vol 250 (6) ◽  
pp. R1065-R1073 ◽  
Author(s):  
R. B. McCall
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Gamma Aminobutyric Acid ◽  
Gaba Antagonists ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Nerve Discharge

The purpose of the present investigation was to determine if gamma-aminobutyric acid (GABA) mediates the baroreceptor-induced inhibition of sympathetic nerve discharge (SND) in dialurethan-anesthetized cats. The GABA antagonists picrotoxin and bicuculline produced marked elevations in arterial blood pressure and inferior cardiac SND. The inhibition of SND observed during pressor responses was occasionally slightly depressed after picrotoxin or bicuculline. Midcollicullar transection blocked or reversed the increase in blood pressure and SND produced by GABA antagonists. Under these conditions, baroreceptor inhibition of SND was not affected by picrotoxin. Microinjections of picrotoxin into the rostral ventrolateral medulla produced increases in arterial blood pressure and SND but failed to affect baroreceptor-induced sympathoinhibition. GABA antagonists given intravenously also failed to affect the baroreceptor-induced inhibition of sympathetically related neurons recorded in the rostral ventrolateral medulla. However, intravenous picrotoxin did antagonize the inhibitory affect of microiontophoretically applied GABA on these neurons. These data provide no evidence to support the contention that GABA mediates the baroreceptor-induced inhibition of SND. The role of GABA in regulating SND is discussed.

Cholecystokinin selectively affects presympathetic vasomotor neurons and sympathetic vasomotor outflow

2002 ◽  
Vol 282 (4) ◽  
pp. R1174-R1184 ◽  
Author(s):  
Daniela M. Sartor ◽  
Anthony J. M. Verberne
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Gastrointestinal Tract ◽  
Sympathetic Nerve ◽  
Vagal Afferents ◽  
Ventrolateral Medulla ◽  
Vasomotor Function ◽  
Arterial Blood ◽  
Potential Mediator ◽  
Nerve Discharge

Cholecystokinin (CCK) is a potential mediator of gastrointestinal vasodilatation during digestion. To determine whether CCK influences sympathetic vasomotor function, we examined the effect of systemic CCK administration on mean arterial blood pressure (MAP), heart rate (HR), lumbar sympathetic nerve discharge (LSND), splanchnic sympathetic nerve discharge (SSND), and the discharge of presympathetic neurons of the rostral ventrolateral medulla (RVLM) in α-chloralose-anesthetized rats. CCK (1–8 μg/kg iv) reduced MAP, HR, and SSND and transiently increased LSND. Vagotomy abolished the effects of CCK on MAP and SSND as did the CCK-A receptor antagonist devazepide (0.5 mg/kg iv). The bradycardic effect of CCK was unaltered by vagotomy but abolished by devazepide. CCK increased superior mesenteric arterial conductance but did not alter iliac conductance. CCK inhibited a subpopulation (∼49%) of RVLM presympathetic neurons whereas ∼28% of neurons tested were activated by CCK. The effects of CCK on RVLM neuronal discharge were blocked by devazepide. RVLM neurons inhibited by exogenous CCK acting via CCK-A receptors on vagal afferents may control sympathetic vasomotor outflow to the gastrointestinal tract vasculature.

scholarly journals Electrical stimulation of the midbrain increases heart rate and arterial blood pressure in awake humans

2002 ◽  
Vol 539 (2) ◽  
pp. 615-621 ◽  
Author(s):  
Judith M. Thornton ◽  
Tipu Aziz ◽  
David Schlugman ◽  
David J. Paterson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Stimulation Of

Midline medullary depressor responses are mediated by inhibition of RVLM sympathoexcitatory neurons in rats

1999 ◽  
Vol 276 (4) ◽  
pp. R1054-R1062 ◽  
Author(s):  
Anthony J. M. Verberne ◽  
Daniela M. Sartor ◽  
Ayse Berke
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Chemical Stimulation ◽  
Ventrolateral Medulla ◽  
Unit Discharge ◽  
Pentobarbital Sodium ◽  
Sympathetic Response ◽  
Long Latency ◽  
Stimulation Of ◽  
Nerve Discharge

Mechanisms underlying the depressor and sympathoinhibitory responses evoked from the caudal medullary raphe (MR) region were investigated in pentobarbital sodium-anesthetized, paralyzed rats. Intermittent electrical stimulation (0.5 Hz, 0.5-ms pulses, 200 μA) of the MR elicited a mixed sympathetic response that consisted of a long-latency sympathoexcitatory (SE) peak (onset = 146 ± 7 ms) superimposed on an inhibitory phase (onset = 59 ± 10 ms). Chemical stimulation of the MR (glutamate; Glu) most frequently elicited depressor responses accompanied by inhibition of sympathetic nerve discharge. Occasionally, these responses were preceded by transient pressor and SE responses. We examined the influence of intermittent electrical stimulation (0.5 Hz, 0.5-ms pulses, 25–200 μA) and Glu stimulation of the MR on the discharge of rostral ventrolateral medulla (RVLM) premotor SE neurons. Peristimulus-time histograms of RVLM unit discharge featured a prominent inhibitory phase in response to MR stimulation (onset = 20 ± 2 ms; duration = 42 ± 4 ms; n = 12 units). Glu stimulation of the MR reduced blood pressure (−37 ± 2 mmHg, n = 19) and inhibited the discharge of RVLM SE neurons (15 of 19 neurons). Depressor and sympathoinhibitory responses elicited by chemical and electrical stimulation of the MR region are mediated by inhibition of RVLM premotor SE neurons and withdrawal of sympathetic vasomotor discharge.

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